The glutathione-S-transferase gene polymorphisms (Gstt1, Gstm1, and Gstp1) in patients with non-allergic nasal polyposis

• Published in: European archives of oto-rhino-laryngology 2010-02, Vol.267 (2), p.227-232
• Main Authors: Özcan, Cengiz, Tamer, Lülüfer, Ates, Nurcan Aras, Görür, Kemal
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; DNA - genetics; Endoscopy; Genetic Predisposition to Disease; Genotype; Glutathione S-Transferase pi - genetics; Glutathione Transferase - genetics; Head and Neck Surgery; Humans; Medical sciences; Medicine; Medicine & Public Health; Middle Aged; Nasal Polyps - diagnosis; Nasal Polyps - enzymology; Nasal Polyps - genetics; Neurosurgery; Otorhinolaryngology; Otorhinolaryngology (head neck, general aspects and miscellaneous); Otorhinolaryngology. Stomatology; Oxidative Stress - genetics; Polymerase Chain Reaction; Polymorphism, Genetic; Rhinology; Tomography, X-Ray Computed; Tumors; Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology
• ISSN: 0937-4477; 1434-4726
• DOI: 10.1007/s00405-009-1066-9

There is an ongoing dilemma about the pathogenesis of nasal polyp (NP). The etiology of NP is multifactorial. Reactive oxygen species and oxidative stress are also suggested to be among the possible factors in NP development. Glutathione- S -transferase (GST) is one of the important detoxifying enzymes. It is not known whether GST plays any role in NP development. We aimed to investigate the relationship between GST subgroup (GSTT1, GSTM1, and GSTP1) polymorphisms, and NP development. Seventy-five patients with NP with or without asthma (NP with asthma: 22, NP without asthma: 53) were used as a study group. As much as 167 healthy individuals were involved as the control group. NP diagnosis was made by nasal endoscopy and paranasal sinus computed tomography (CT). NP was defined as the presence of endoscopically visible bilateral polyps originated from the middle meatus to the nasal cavity and affecting more than one paranasal sinus confirmed by CT. Blood was collected in EDTA-containing tubes and DNA was extracted from the leukocytes. The genotyping of polymorphisms of GSTT1, GSTM1, and GSTP1 were done using real time polymerase chain reaction. Chi-square (χ 2 ) and Fisher’s ( F ) exact tests were used for statistical evaluation. A 2-fold increased risk of NP could be found in individuals with the GSTT1 null genotype (OR = 2.03, 95% CI = 1.03–4.011). The distribution of GSTM1 null genotypes was not significantly different between the NP patients and controls and there was also no significance between the GSTP1 genotypes and NP. In conclusion, GST gene polymorphisms may be important in pathogenesis of NP. Additional studies which include larger study groups in different geographic localizations may be more useful to evaluate association with GST polymorphism and NP.